Restoring of insulin-synthesizing cell pool by means of macrophage activity modulation can be a promising direction in the treatment of diabetes mellitus. Modeling of type 2 diabetes mellitus in rats (110 mg / kg of nicotinamide and 65 mg / kg of streptozotocin) caused a spontaneous compensatory increase in the number of extra islet insulin-producing cells up to 30 days, followed by a decrease in the number of these cells by 60 days without enhancing their functional activity. Modulation of macrophage activity with the administration of aminophthalhydrazide (2 mg / kg, 20 injections) to diabetic rats was accompanied by an increase in the number of the extra islet insulin-producing cells, the accumulation of insulin in all the studied groups of these cells, and a reduction in hyperglycemia.